Faith writes:
I don't know if I'm tired, burning out on this topic, unable to make sense of the technical language or what, but I can't get anything out of what you are saying.
I see mutations as mistakes. Great if sometimes they don't destroy something. Haven't seen any evidence that all these alleles do anything new, so I assume they just do whatever the original alleles did for any given gene.
You would have seen the evidence in some of the material presented had you understood it.
What the HLA-B proteins do is bind with peptides (parts of other proteins), and transport them to the surface of cells for inspection by killer T-cells which, if they identify what's presented as foreign, will attack the invader. The different alleles bind to different and sometimes overlapping ranges of peptides, and the intruders will have many peptides, so there's a good chance that an allele can latch onto something in most pathogens.
Picture a burglar (HLA-B allele) with a set of skeleton keys (peptide binding repetoire) and many mansions (pathogens) with many locked doors per. mansion (peptides). For most mansions, the burglar can open at least one door, but if he works with a friend who has a different set of skeleton keys, they have more chance of being able to open at least one door (heterozygosity).
But the mansion owners keep changing the locks, and sometimes they can come up with a set of locks that cannot be opened by either set of keys. The analogy only goes so far, but what we perceive as regional or global disease epidemics can be when a mutant pathogen doesn't happen to have any peptides that are locked onto efficiently by most of the common alleles. When that happens, the strain is successful and can multiply exploiting our bodies. However, because the intruders have many peptides (locked doors) it's hard for them to avoid all the many alleles/burglars in the neighbourhood on all of their peptides, because of the collective range of all the sets of skeleton keys (binding repetoires/ranges) in the population as a whole.
The most succesful pathogen strains will be good at evading common alleles because that's why they have become successful (positive selection for not having matching peptides with common HLA-B alleles). But they won't be likely to have adaptations to all the rare alleles, so any alleles that can deal with the problem face positive selection over time against the more common ones. When they themselves become common, then some successful mutant pathogens may have adapted to avoid them, and off we go on a new cycle of balancing selection.
Faith writes:
Time since Adam and Eve is irrelevant since things started over with the Flood and that's where counting alleles would have to begin I suppose. How could we know if any of the indiviudals on the Ark had mutant alleles anyway? All that's needed to create all the known diversity since the Ark is two alleles per gene shared by all individuals.
Known diversity? Known to whom?
Faith writes:
If there are too many mutations to have occurred in the last 4500 years since the Ark, what can I do but assume that for some reason they occurred a lot faster than usual since then, at least in the immune system which appears to be unusual for its great number.
A super high rate of neutral mutations gives a different distribution pattern from the one we see. However, YECs do need to argue for past high mutation rates for many animals, including humans, because the divergence on genomes within "kinds" is so much more than the model would predict on normal rates
Faith writes:
But I think I'm burned out on this topic.
It's a sub-thread/topic, really. Why not try to address something like the niche filling of the species that evolved (or devolved) from the "kinds" on the Ark? Surely loads of natural selection on phenotypes is required for all this. How can specialists like polar bears and
Plasmodium falciparum match their environments so well without it?
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